中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2010年
12期
1193-1196,1200
,共5页
安雅臣%王玉浔%陈乃耀%申娜%王大力%赵晓晶%张江%李春玲%彭延波%高素玲%常丽莎%张丽%薛新宏%陈瑞英
安雅臣%王玉潯%陳迺耀%申娜%王大力%趙曉晶%張江%李春玲%彭延波%高素玲%常麗莎%張麗%薛新宏%陳瑞英
안아신%왕옥심%진내요%신나%왕대력%조효정%장강%리춘령%팽연파%고소령%상려사%장려%설신굉%진서영
间质干细胞移植%颅脑损伤%神经生长因子%脑源性神经营养因子
間質榦細胞移植%顱腦損傷%神經生長因子%腦源性神經營養因子
간질간세포이식%로뇌손상%신경생장인자%뇌원성신경영양인자
Mesenchymal stem cell transplantation%Craniocerebral trauma%Nerve growth factor%Brain-derived neurotrophic factor
目的 观察TBI后静脉注射人脐血间充质干细胞(CB-MSCs)对NGF、BDNF表达的影响,探讨其脑保护的作用机制.方法 清洁级健康雄性SD大鼠90只采用完全随机数字表法分为假手术组、损伤组和治疗组,每组30只.损伤组和治疗组采用改进的Feeney自由落体法制作大鼠TBI模型,假手术组只开骨窗,不撞击硬脑膜.治疗组尾静脉注入3×106个Brdu标记的CB-MSCs,损伤组及假手术组注入等体积的PBS液.在移植后3、7、14、21、28 d,采用HE染色、免疫组化染色、原位杂交法对TBI大鼠脑组织形态学变化、Brdu标记情况、NGF和BDNF表达情况进行检测.结果 假手术组仅有极少量的NGF、BDNF阳性表达细胞.损伤组表达明显增加,以损伤周边区最为明显,注射后14d达到高峰(NGFA值为8.35±1.07,BDNFA值为9.01±1.74),之后逐渐下降,但仍高于假手术组,差异有统计学意义(P＜0.05).治疗组表达趋势与损伤组相同,14d达高峰后,21 d、28 d阳性表达明显下降;各时间点均高于损伤组与假手术组,差异有统计学意义(P＜0.05).结论 在TBI中,静脉注射CB-MSCs可以增加损伤局部NGF、BDNF的分泌,改善局部微环境,促进神经元的修复.
目的 觀察TBI後靜脈註射人臍血間充質榦細胞(CB-MSCs)對NGF、BDNF錶達的影響,探討其腦保護的作用機製.方法 清潔級健康雄性SD大鼠90隻採用完全隨機數字錶法分為假手術組、損傷組和治療組,每組30隻.損傷組和治療組採用改進的Feeney自由落體法製作大鼠TBI模型,假手術組隻開骨窗,不撞擊硬腦膜.治療組尾靜脈註入3×106箇Brdu標記的CB-MSCs,損傷組及假手術組註入等體積的PBS液.在移植後3、7、14、21、28 d,採用HE染色、免疫組化染色、原位雜交法對TBI大鼠腦組織形態學變化、Brdu標記情況、NGF和BDNF錶達情況進行檢測.結果 假手術組僅有極少量的NGF、BDNF暘性錶達細胞.損傷組錶達明顯增加,以損傷週邊區最為明顯,註射後14d達到高峰(NGFA值為8.35±1.07,BDNFA值為9.01±1.74),之後逐漸下降,但仍高于假手術組,差異有統計學意義(P＜0.05).治療組錶達趨勢與損傷組相同,14d達高峰後,21 d、28 d暘性錶達明顯下降;各時間點均高于損傷組與假手術組,差異有統計學意義(P＜0.05).結論 在TBI中,靜脈註射CB-MSCs可以增加損傷跼部NGF、BDNF的分泌,改善跼部微環境,促進神經元的脩複.
목적 관찰TBI후정맥주사인제혈간충질간세포(CB-MSCs)대NGF、BDNF표체적영향,탐토기뇌보호적작용궤제.방법 청길급건강웅성SD대서90지채용완전수궤수자표법분위가수술조、손상조화치료조,매조30지.손상조화치료조채용개진적Feeney자유락체법제작대서TBI모형,가수술조지개골창,불당격경뇌막.치료조미정맥주입3×106개Brdu표기적CB-MSCs,손상조급가수술조주입등체적적PBS액.재이식후3、7、14、21、28 d,채용HE염색、면역조화염색、원위잡교법대TBI대서뇌조직형태학변화、Brdu표기정황、NGF화BDNF표체정황진행검측.결과 가수술조부유겁소량적NGF、BDNF양성표체세포.손상조표체명현증가,이손상주변구최위명현,주사후14d체도고봉(NGFA치위8.35±1.07,BDNFA치위9.01±1.74),지후축점하강,단잉고우가수술조,차이유통계학의의(P＜0.05).치료조표체추세여손상조상동,14d체고봉후,21 d、28 d양성표체명현하강;각시간점균고우손상조여가수술조,차이유통계학의의(P＜0.05).결론 재TBI중,정맥주사CB-MSCs가이증가손상국부NGF、BDNF적분비,개선국부미배경,촉진신경원적수복.
Objective To investigate the effect of transplantation of human umbilical cord blood mesenchymal stem cells (CB-MSCs) on the levels of NGF and BDNF in rats with traumatic brain injury (TBI) and explore its possible mechanism of cerebral protection. Methods Ninety healthy male SD rats were equally randomized into sham-operated group, injury control group and treatment group.TBI models in the injury control group and treatment group were induced by the improved device of Feeney weight-dropping; the rats in the treatment group were injected Brdu-labeled 3×106 CB-MSCs solved in 1ml PBS by rat-tail vein, while the rats in the sham-operated group and the injury control group were injected the equal volume of PBS solution. No immunosuppressive agents were used in all the rats.HE staining, immunohistochemistry, in-situ hybridization were employed, respectively, to detect the morphological changes, Brdu positive cells, expressions of BDNF and NGF on the 3rd, 7th, 14th, 21st and 28th d of injection. Results Only a very small number of nerve cells were BDNF and/or NGF positive in the sham-operated group. Substantial BDNF and/or NGF positive cells in the injury control group were noted in the surrounding brain damaged area following traumatic brain injury, which peaked at their levels on about 14 d of injection (the A value of NGF=8.35±1.07, that of BDNF=9.01±1.74), following by a gradual decline; however, significant difference was still noted as compared with that in the sham-operated group (P＜0.05). BDNF and/or NGF-positive cells significantly increased in the treatment group, especially in the surrounding brain injured areas; their levels peaked on the 14th d of injection,following by a gradual decline on the 21st and 28th d, but they were still higher than those in the injury control group and sham-operated group at each time points (P＜0.05). Conclusion Transplantation of CB-MSCs can increase the secretion of BDNF and NGF in rats with TBI, improve the local micro-damage environment and promote the repair of neurons.
